sirolimus and phosphoramide-mustard

sirolimus has been researched along with phosphoramide-mustard* in 1 studies

Other Studies

1 other study(ies) available for sirolimus and phosphoramide-mustard

Article	Year
Phosphoramide mustard induces autophagy markers and mTOR inhibition prevents follicle loss due to phosphoramide mustard exposure. Reproductive toxicology (Elmsford, N.Y.), 2017, Volume: 67 Phosphoramide mustard (PM) is an ovotoxic metabolite of cyclophosphamide. Postnatal day 4 Fisher 344 rat ovaries were exposed to vehicle control (1% DMSO) or PM (60μM)±LY294002 or rapamycin for 2 or 4 d. Transmission election microscopy revealed abnormally large golgi apparatus and electron dense mitochondria in PM-exposed ovaries prior to and at the time of follicle depletion. PM exposure increased (P<0.05) mRNA abundance of Bbc3, Cdkn1a, Ctfr, Edn1, Gstp1, Nqo1, Tlr4, Tnfrsfla, Txnrd1 and decreased (P<0.05) Casp1 and Il1b after 4d. PM exposure increased (P<0.1) BECN1 and LAMP, decreased (P<0.1) ABCB1 and did not alter ABCC1 protein. LY294002 did not impact PM-induced ovotoxicity, but decreased ABCC1 and ABCB1 protein. Rapamycin prevented PM-induced follicle loss. These data suggest that the mammalian target of rapamycin, mTOR, may be a gatekeeper of PM-induced follicle loss. Topics: Animals; Animals, Newborn; Antineoplastic Agents, Alkylating; Autophagy; Female; Golgi Apparatus; In Vitro Techniques; Mitochondria; Ovarian Follicle; Ovary; Phosphoramide Mustards; Rats, Inbred F344; Sirolimus; TOR Serine-Threonine Kinases	2017

Article

Year

Phosphoramide mustard induces autophagy markers and mTOR inhibition prevents follicle loss due to phosphoramide mustard exposure.

Reproductive toxicology (Elmsford, N.Y.), 2017, Volume: 67

Phosphoramide mustard (PM) is an ovotoxic metabolite of cyclophosphamide. Postnatal day 4 Fisher 344 rat ovaries were exposed to vehicle control (1% DMSO) or PM (60μM)±LY294002 or rapamycin for 2 or 4 d. Transmission election microscopy revealed abnormally large golgi apparatus and electron dense mitochondria in PM-exposed ovaries prior to and at the time of follicle depletion. PM exposure increased (P<0.05) mRNA abundance of Bbc3, Cdkn1a, Ctfr, Edn1, Gstp1, Nqo1, Tlr4, Tnfrsfla, Txnrd1 and decreased (P<0.05) Casp1 and Il1b after 4d. PM exposure increased (P<0.1) BECN1 and LAMP, decreased (P<0.1) ABCB1 and did not alter ABCC1 protein. LY294002 did not impact PM-induced ovotoxicity, but decreased ABCC1 and ABCB1 protein. Rapamycin prevented PM-induced follicle loss. These data suggest that the mammalian target of rapamycin, mTOR, may be a gatekeeper of PM-induced follicle loss.

Topics: Animals; Animals, Newborn; Antineoplastic Agents, Alkylating; Autophagy; Female; Golgi Apparatus; In Vitro Techniques; Mitochondria; Ovarian Follicle; Ovary; Phosphoramide Mustards; Rats, Inbred F344; Sirolimus; TOR Serine-Threonine Kinases

2017